is provided by the state boards of medicine. FDA CFR Title 21 part 1271 concerns the regulation of human cells and cellular products. It states the physician is in compliance if the cell products are removed and re-implanted into the same patient during the same procedure. These cells must also be “minimally manipulated”. This has been interpreted to mean that centrifugation and cell selection is permissible but cell expansion and tissue culture is not. It should be recognized that regulations are likely to change in areas such as these where technology is evolving quickly.
CONCLUDING REMARKS
Autologous fat transplantation has great appeal for facial rejuvenation and soft tissue augmentation because it avoids complications of foreign material and requires no surgical scars. However, the technique has been limited by the unpredictability of graft survival.1-3
The above method of cell-assisted facial fat transfer combines optimal harvesting and implantation of adipocytes with the addition of growth factors from PRP and a cell population derived from the enzymatic digestion and centrifugation of adipose tissue SVF. This SVF contains ADSCs, pre-adipocytes, endothelial cells, fibroblasts, macrophages, NK cells, and others. The ADSCs offer proliferative potential and the ability to differentiate into mature adipocytes and endothelial structures, as well as, secrete cytokines and growth factors.5-8
In the cell augmented lipotransfer (CAL) strategy, ADSCs are used to increase angiogenesis, improve graft survival, and reduce postoperative atrophy. These cells (found in SVF) are added to intact adipocytes, which provide volume and act as a living scaffold.12
A potential improvement in the efficacy of growth factor and cell assisted lipotransfer is likely due to ADSCs differentiating into mature adipocytes as cell turnover progresses, as well as other ADSCs differentiating into vascular endothelial cells contributing to neo-angiogenesis during the healing process. This results in increased microvasculature, decreased central necrosis, and prolonged survival of the transplanted adipocytes.6,8-10,12
REFERENCES
1.Coleman SR. Structural fat grafts: The ideal filler. Clin Plast Surg. 2001;28:111-119.
2.Shiffman MA, Mirafati S. Fat transfer techniques: The effects of harvest and transfer methods on adipocytes viability and review of the literature. Dermatol Surg. 2001;27:819-826.
3.Kurita M, Matsumoto D, Shigeruro T. Influences of centrifugation on cells and tissues in liposuction aspirate. Optimized centrifugation for lipotransfer and cell isolation. Plast Reconstr Surg. 2008;7: 211-228.
4.Carpenda CA, Ribiero MT. Percentage of grafts vs. injected volume in adipose autotransplants. Aesthetic Plastic Surg. 1994;18:17-19.
5.Zuk PA, Zhu M, Mizuno H, Huang J. Human adipose tissue is a source of multipotent stem cells. Mol Biol Cell. 2005;13:4279-4294.
6.Moseley TA, Zhu M, Hedrick MH. Adipose derived stem and progenitor cells as fillers in plastic and reconstructive surgery. Plast Reconstr Surg. 2006;118 (3 supplement):1215-1285.
7.Planat-Bernard V, Silvestre JS, Cousin B. Plasticity of human adipose lineage cells toward endothelial cells: physiological and therapeutic perspective. Circulation 2004;109:656-663.
8.Strawford A, Autelo F, Christianseu M. Adipose triglyceride turnover, cell proliferation in humans measured with 2 H2O. AmJ Physiol Endocrinol Metab. 2004;256:E 577-588.
9.Yoshimura K, Sato K, Aoi N, Cell assisted lipotransfer for cosmetic breast augmentation – supportive use of adipose derived stem-stromal cells. Aesthetic Plast Surg. 2008;32:48-55.
10.Yoshimura K, Sato K, Aoi N, Masakazu K. Cell assisted lipotransfer for facial lipoatrophy: efficacy of clinical use of adipose derived stem cells. Dermatol Surg. 2006;34:1178-1185.
11.Mojallal N. Improvement in skin quality after fat grafting: clinical observations and an animal study. Plast reconstruct Surg. 2009;124:765-774.
12.Matsumoto D, Sato K, Gonda R, Takakai Y. Cell assisted lipotransfer: Supportive use of human adipose derived cells for soft tissue augmentation. Tissue Engineering. 2006;3375-3382.
ABOUT THE AUTHOR
Dr. Robert Bowen is an Internal Medicine and Pulmonary specialist, Board Certified in Cosmetic Laser Surgery by the American Board of Laser Surgery. He is a Fellow of the American Society of Laser Medicine and Surgery and has published research articles on laser medicine. Dr. Bowen is a Diplomate of the American Board of Anti-Aging Medicine and a graduate of the Aesthetic Medicine Fellowship.
Chapter 3
Innovations in the Treatment of Chronic Wounds
Robert E. Bowen, M.D., FCCP, FSLMS
Clinical Associate Professor, WVU-East
Medical Director, The Center for Positive Aging, Martinsburg, WV
ABSTRACT
Healing of wounds is a complex process that most often proceeds in an orchestrated fashion resulting in repair of the injured area. When this orchestration proceeds in a disordered fashion then the healing process may result in an over-expression of fibroblasts (resulting in a hypertrophic scar or keloid) or inability to form new tissue (chronic wound). Hypertrophic scars are commonly seen as sequelae of thermal injuries (burns) and chronic wounds are often seen in patients with arterial and venous insufficiency and diabetes.
Previous approaches to these problems have resulted only in marginal improvement in care. Newly developed innovations in wound care are discussed as are future directions for research.
INTRODUCTION
Thermal Injuries
Advances in the treatment of serious burns have been achieved by centralizing treatment in “burn units” where multiple specialties including surgery, infectious disease, and critical care medicine have contributed to improvement in survival. This has been achieved by more effective management of the hypermetabolic state, infection control and nutrition. As a result of increased survival from serious burns, more patients are left with the sequelae of the resultant cutaneous and psychological scars.
The fibroblastic reaction to a thermal injury includes increased levels of inflammatory cytokines including interleukin-4 (IL-4), which increases several weeks after injury and continues for several months. In this stage of disordered healing there is increased collagen formation and decreased collagenolysis resulting in the formation of a hypertrophic scar.
Lasers have been used in the treatment of these hypertrophic scars with varying degrees of success. The SOFT™ method was developed to address the issue of the heterogeneity of the thickness of such scars. With this approach each region of a scar is treated with a fractional ablative laser at a depth sufficient to penetrate the scar.1 This both reduces the volume of the scar tissue and creates channels that may allow resident and circulating stem cells to gain access to the scar and help normalize the structure of the tissue. Early case studies have established the credibility of this concept and further improvement of efficacy can be achieved by defining the optimal:
•Density of treatment to the area (pitch);
•Quantity
